141 research outputs found
Neutrino spin rotation in dense matter and electromagnetic field
Exact solutions of the Dirac--Pauli equation for massive neutrino with
anomalous magnetic moment interacting with dense matter and strong
electromagnetic field are found. The complete system of neutrino wavefunctions,
which show spin rotation properties are obtained and their possible
applications are discussed.Comment: 11 pages, latex, misprints are correcte
Screening of cosmological constant for De Sitter Universe in non-local gravity, phantom-divide crossing and finite-time future singularities
We investigate de Sitter solutions in non-local gravity as well as in
non-local gravity with Lagrange constraint multiplier. We examine a condition
to avoid a ghost and discuss a screening scenario for a cosmological constant
in de Sitter solutions. Furthermore, we explicitly demonstrate that three types
of the finite-time future singularities can occur in non-local gravity and
explore their properties. In addition, we evaluate the effective equation of
state for the universe and show that the late-time accelerating universe may be
effectively the quintessence, cosmological constant or phantom-like phases. In
particular, it is found that there is a case in which a crossing of the phantom
divide from the non-phantom (quintessence) phase to the phantom one can be
realized when a finite-time future singularity occurs. Moreover, it is
demonstrated that the addition of an term can cure the finite-time future
singularities in non-local gravity. It is also suggested that in the framework
of non-local gravity, adding an term leads to possible unification of the
early-time inflation with the late-time cosmic acceleration.Comment: 42 pages, no figure, version accepted for publication in General
Relativity and Gravitatio
Neutron Majorana mass from exotic instantons
We show how a Majorana mass for the Neutron could result from
non-perturbative quantum gravity effects peculiar to string theory. In
particular, "exotic instantons" in un-oriented string compactifications with
D-branes extending the (supersymmetric) standard model could indirectly produce
an effective operator delta{m} n^t n+h.c. In a specific model with an extra
vector-like pair of `quarks', acquiring a large mass proportional to the string
mass scale (exponentially suppressed by a function of the string moduli
fields), delta{m} can turn out to be as low as 10^{-24}-10^{-25} eV. The
induced neutron-antineutron oscillations could take place with a time scale
tau_{n\bar{n}} > 10^8 s, that could be tested by the next generation of
experiments. On the other hand, proton decay and FCNC's are automatically
strongly suppressed and are compatible with the current experimental limits.
Depending on the number of brane intersections, the model may also lead to the
generation of Majorana masses for R-handed neutrini. Our proposal could also
suggest neutron-neutralino or neutron-axino oscillations, with implications in
UCN, Dark Matter Direct Detection, UHECR and Neutron-Antineutron oscillations.
This suggests to improve the limits on neutron-antineutron oscillations, as a
possible test of string theory and quantum gravity.Comment: 35 pages, 11 figures. More comments on neutron-neutralino mixin
QUANTITATIVE AND QUALITATIVE ANALYSIS HIERARCHY
This article studied the methods of quantitative and qualitative analysis of hierarchies and made the analysis of the existing hierarchy
Protein kinase Cepsilon is important for migration of neuroblastoma cells
<p>Abstract</p> <p>Background</p> <p>Migration is important for the metastatic capacity and thus for the malignancy of cancer cells. There is limited knowledge on regulatory factors that promote the migration of neuroblastoma cells. This study investigates the hypothesis that protein kinase C (PKC) isoforms regulate neuroblastoma cell motility.</p> <p>Methods</p> <p>PKC isoforms were downregulated with siRNA or modulated with activators and inhibitors. Migration was analyzed with scratch and transwell assays. Protein phosphorylation and expression levels were measured with Western blot.</p> <p>Results</p> <p>Stimulation with 12-<it>O</it>-tetradecanoylphorbol-13-acetate (TPA) induced migration of SK-N-BE(2)C neuroblastoma cells. Treatment with the general protein kinase C (PKC) inhibitor GF109203X and the inhibitor of classical isoforms Gö6976 inhibited migration while an inhibitor of PKCβ isoforms did not have an effect. Downregulation of PKCε, but not of PKCα or PKCδ, with siRNA led to a suppression of both basal and TPA-stimulated migration. Experiments using PD98059 and LY294002, inhibitors of the Erk and phosphatidylinositol 3-kinase (PI3K) pathways, respectively, showed that PI3K is not necessary for TPA-induced migration. The Erk pathway might be involved in TPA-induced migration but not in migration driven by PKCε. TPA induced phosphorylation of the PKC substrate myristoylated alanine-rich C kinase substrate (MARCKS) which was suppressed by the PKC inhibitors. Treatment with siRNA oligonucleotides against different PKC isoforms before stimulation with TPA did not influence the phosphorylation of MARCKS.</p> <p>Conclusion</p> <p>PKCε is important for migration of SK-N-BE(2)C neuroblastoma cells. Neither the Erk pathway nor MARCKS are critical downstream targets of PKCε but they may be involved in TPA-mediated migration.</p
A Cell Motility Screen Reveals Role for MARCKS-Related Protein in Adherens Junction Formation and Tumorigenesis
Invasion through the extracellular matrix (ECM) is important for wound healing, immunological responses and metastasis. We established an invasion-based cell motility screen using Boyden chambers overlaid with Matrigel to select for pro-invasive genes. By this method we identified antisense to MARCKS related protein (MRP), whose family member MARCKS is a target of miR-21, a microRNA involved in tumor growth, invasion and metastasis in multiple human cancers. We confirmed that targeted knockdown of MRP, in both EpRas mammary epithelial cells and PC3 prostate cancer cells, promoted in vitro cell migration that was blocked by trifluoperazine. Additionally, we observed increased immunofluoresence of E-cadherin, β-catenin and APC at sites of cell-cell contact in EpRas cells with MRP knockdown suggesting formation of adherens junctions. By wound healing assay we observed that reduced MRP supported collective cell migration, a type of cell movement where adherens junctions are maintained. However, destabilized adherens junctions, like those seen in EpRas cells, are frequently important for oncogenic signaling. Consequently, knockdown of MRP in EpRas caused loss of tumorigenesis in vivo, and reduced Wnt3a induced TCF reporter signaling in vitro. Together our data suggest that reducing MRP expression promotes formation of adherens junctions in EpRas cells, allowing collective cell migration, but interferes with oncogenic β-catenin signaling and tumorigenesis
Myelin-mediated inhibition of oligodendrocyte precursor differentiation can be overcome by pharmacological modulation of Fyn-RhoA and protein kinase C signalling
Failure of oligodendrocyte precursor cell (OPC) differentiation contributes significantly to failed myelin sheath regeneration (remyelination) in chronic demyelinating diseases. Although the reasons for this failure are not completely understood, several lines of evidence point to factors present following demyelination that specifically inhibit differentiation of cells capable of generating remyelinating oligodendrocytes. We have previously demonstrated that myelin debris generated by demyelination inhibits remyelination by inhibiting OPC differentiation and that the inhibitory effects are associated with myelin proteins. In the present study, we narrow down the spectrum of potential protein candidates by proteomic analysis of inhibitory protein fractions prepared by CM and HighQ column chromatography followed by BN/SDS/SDS–PAGE gel separation using Nano-HPLC-ESI-Q-TOF mass spectrometry. We show that the inhibitory effects on OPC differentiation mediated by myelin are regulated by Fyn-RhoA-ROCK signalling as well as by modulation of protein kinase C (PKC) signalling. We demonstrate that pharmacological or siRNA-mediated inhibition of RhoA-ROCK-II and/or PKC signalling can induce OPC differentiation in the presence of myelin. Our results, which provide a mechanistic link between myelin, a mediator of OPC differentiation inhibition associated with demyelinating pathologies and specific signalling pathways amenable to pharmacological manipulation, are therefore of significant potential value for future strategies aimed at enhancing CNS remyelination
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